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Kanthlal S K,
Prahala P.R,
Samina Sameer,
Sandra Pillai,
Kiran KJ,
Prasobh GR,
Anusha Jasmin R J,
- Professor, Sree Krishna College of Pharmacy and Research Centre, Parassala, Thiruvananthapuram, Kerala, India
- Student, Sree Krishna College of Pharmacy and Research Centre, Parassala, Thiruvananthapuram, kerala, India
- Student, Sree Krishna College of Pharmacy and Research Centre, Parassala, Thiruvananthapuram, kerala, India
- Student, Sree Krishna College of Pharmacy and Research Centre, Parassala, Thiruvananthapuram, Kerala, India
- Student, Sree Krishna College of Pharmacy and Research Centre, Parassala, Thiruvananthapuram, Kerala, India
- Student, Sree Krishna College of Pharmacy and Research Centre, Parassala, Thiruvananthapuram, Kerala, India
- Student, Sree Krishna College of Pharmacy and Research Centre, Parassala, Thiruvananthapuram, Kerala, India
Abstract
Drug-induced immune-mediated nephritis (DI-IMN) has become a more widely known cause of acute kidney injury (AKI), with the potential for development to chronic kidney disease if not detected and treated promptly. T-cell hypersensitivity to pharmaceuticals such antibiotics, proton pump inhibitors, nonsteroidal anti-inflammatory drugs, and immunological drugs are the maor causes for it. Beyond clinical burden, DI-IMN is a reflection of intricate molecular interactions that sustain interstitial inflammation and tubular injury. These interactions include haptenization and neoantigen creation, antigen presentation, costimulatory signaling, and cytokine-chemokine networks. Conventional biomarkers, such as proteinuria and serum creatinine, are not sensitive enough to detect early disease. Novel urine and serum indicators (such as soluble CD163, NGAL, MCP-1, and KIM-1) and multi-omics techniques provide better phenotyping, therapy monitoring, and earlier detection. Renal biopsy with immunophenotyping remains the diagnostic cornerstone, but the combination of genetic profiling, pharmacogenomics, and AI-based risk models promises more precise, less intrusive approaches. This review synthesizes epidemiology, immunopathogenesis, and drug-specific patterns of DI-IMN, highlighting diagnostic challenges and translational opportunities. We emphasize early drug withdrawal and timely immunosuppression to enhance renal recovery, along with reno-protective measures. Future directions focus on personalized medicine, and real-time monitoring is required to mitigate long-term renal morbidity and improve patient outcomes who exposed to high-risk medications.
Keywords: Nephritis, Immune reaction, T-cell, cytokine-chemokine, Personalized medicine
Kanthlal S K, Prahala P.R, Samina Sameer, Sandra Pillai, Kiran KJ, Prasobh GR, Anusha Jasmin R J. DRUG INDUCED IMMUNE MEDIATED NEPHRITIS: MOLECULAR MECHANISM , PATHWAYS AND CLINICAL IMPLICATIONS. International Journal of Toxins and Toxics. 2026; 03(01):-.
Kanthlal S K, Prahala P.R, Samina Sameer, Sandra Pillai, Kiran KJ, Prasobh GR, Anusha Jasmin R J. DRUG INDUCED IMMUNE MEDIATED NEPHRITIS: MOLECULAR MECHANISM , PATHWAYS AND CLINICAL IMPLICATIONS. International Journal of Toxins and Toxics. 2026; 03(01):-. Available from: https://journals.stmjournals.com/ijtt/article=2026/view=236729
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International Journal of Toxins and Toxics
| Volume | 03 |
| 01 | |
| Received | 22/01/2026 |
| Accepted | 30/01/2026 |
| Published | 31/01/2026 |
| Publication Time | 9 Days |
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